Infectious Diseases

Question 1

Virulent Newcastle Diseases in Chickens. Associated Clinical signs ?

Answer 1

1. sudden death + increase death loss in flocks
2. respiratory symptoms (sneezing, gasping for air, nasal discharge and coughing)
3. greenish watery diarrhea, lethargy, tremors and dropped wings
4. torticollis, circling, complete stiffness, swelling around eyes and neck

Pilny and Reavill_2020_Emerging and Re- emerging Diseases of selected avian species

Question 2

Sarcocystis calchasi
A: intermediate host?
B: definitive host?
C: Clinical signs?

Answer 2

A: pigeons (+ several psittacine hosts -including princess parrots and cockatoos)
B: northern goshawk
+ European sparrohawk
C: CNS signs: torticollis, nystagmus, ataxia, inability to stand, star gazing, ophistotonus; pigeon diphasic diseases: first PU, diarrhea, lethargy later CNS signs
Pilny and Reavill_2020_Emerging and Re- emerging Diseases of selected avian species

Question 3

Schistosomes
A: which family of parasites?
B: intermediate host?

Answer 3

A: trematodes
B: snails

Pilny and Reavill_2020_Emerging and Re- emerging Diseases of selected avian species

Question 4

Antifungals:
name the 3 main classes of Antifungals, give examples, and name their mode of action?

Answer 4

1. Polyenes (Amphotericin B): interference with membrane barrier function, by sterol binding that results in leckage of fungal cells through creation of transmembrane channels–> leads to cell death
2. Azole (Itraconazole. Fluconazole. Voriconazole): interrupts biosynthese of ergosterol needed for fungal cell membrane function –>depleting cell stores while accumulating the unneeded sterol
   (Speer: Azole: inhibit cytochrome P450-dependent 14 alpha sterol demethylase required for conversion of lanosterol to ergosterol, exposed fungi: depleted of ergosterol and accumulate 14 alpha methylated sterols disruption of membrane structure and function—inhibit fungal growth )
3. Allylamines (Terbinafin): inhibits ergosterol synthesis by blocking squalene monooxygenase–> (speer: epioxidase)intracellular accumulation of toxic squalene
   Antifungals in Birds (Zoo& Wildlife Medicine 9th edition)

Question 5

ABV
How many genotypes for psittacine birds exist?

Which is the most common?

What is the nature of the Virus (nonenveloped/enveloped RNA/DNA)?

Answer 5

8 genotypes
ABV 4, followed by ABV 2
Nonenveloped RNA

Question 6

Why is the antigangliosid AB theory in regard of the Bornavirus pathogenesis not fully accepted/ proven ?

Answer 6

In experimental infection antigangliosid AB not detectable in confirmed PDD cases and also poor connection in clinical cases

Question 7

Bornavirus- What would be a typical p.m pathohistological finding ?

Answer 7

Lymphoplasmacytic infiltration in the ganglia of the nerves

Question 8

Bornavirus:
Which sample material would you prefer for Bornavirus PCR form a living bird?

Which sample material would you prefer for Bornavirus PCR form a death bird?

Answer 8

1 sample crop (oropharnygeal) + cloaca (seems superior) also possible: Blood, feather calamus, feces

Brain and retinal tissue (also adrenal gland, proventriculus, ventriculus)

Question 9

You tested a Grey parrot without clinical signs of diseases routinely for Bornavirus AG and AB, you could a positive AG (PCR )result but negative AB titers.
How would you judge the results? How to proceed with this case?

Are birds able to clear ABV infections?

With a positive ABV bird,without clinical signs, what would be the prognosis? What would you recommend the owner?

Answer 9

Retest in 4-6 week- bird kept seperated till than; shedding without seroconversion would be possible - can also be seen in experimental infections

Yes they are

Unkown prognosis, everthing is possible
Avoid stress, keep seperated from a negative flock , whatch for cearly clinical signs

Question 10

A 6 year old male blue and gold macaw (Ara ararauna) is brought for a second opinion The
bird has been exhibiting lethargy, undigested seeds in the faeces over the past week. The
owner has taken the bird to her regular veterinarian who did a hematology and biochemistry, a
radiograph, a crop cytology, a fecal cytology/coproscopy and a crop biopsy.
1. What is the differential diagnosis for such radiographic lesion ?
2. The referring vet has performed a crop biopsy. The histological result was unremarkable.
What is your interpretation?
3. What would be the next diagnostic step ? Cite 4 different exams.

Answer 10

Proventricular dilatation diseases, Avian Bornavirus , foreign body, funga/bacterial/parasitic(nasopharynx) infections, heavymetal (zinc), neoplasia, mass ,granuloma
2 crop Biopsy is not sensitive tool
Control radiography, prov/ventr biopsy, heavy metals tests, Bornavirus AG + serology,

Question 11

A parrot breeder has had proventricular dilatation disease cases in his collection and want to
setup an ABV-negative flock.
What is the first measure to take ? How do you organize the collection in terms of
compartment ?
A breeding pair has a positive male and a negative female. The breeder do not want to
separate them. What is your advice regarding the pair ? What is your advice regarding their
offsprings ?
According to Lierz et al, what are the conditions to consider a group of bird as cleared from
infection ?

Answer 11

discuss with owner- long , expensive and frustrating ; , test all birds with crop and cloacal swab for Bornavirus AG /RT PCR) and blood for serology
organize birds: negative, positive, questionable
breeding pair: treat them as pos birds; eggs taken away- disinfect (3 % hydrogen peroxid) , hatched chicks separated single housed and repeatedly tested (4,6 and 8 weeks after hatch) because of maternal AB ´) as soon as repeated negative can be grouped/ transferred to foster parents ; alternative: put to neg foster parents- but poss a risk to foster parents- make only sense when less valuable foster parents and very valuable parents
2 consecutive tests 4-6 weeks apart of all birds in the group

Question 12

Avian bornavirus and proventricular dilation disease
This African grey parrot is presented for lethargy and change of color from the feathers. You want to rule out PBFD infection.
Which test do you perform ?
Which other pathological findings apart from dermatological findings, would you expect with an active PBFD infection ?
This parrot has been in contact with a cockatiel in the same household. What is the likelihood that this cockatiel develop the disease ?

Answer 12

Cloacal and Cropd swab for AG (RT PCR ) and blood for serology- at least to consecutive tests 4-6 weeks apart/ PCR on blood and feather !
Leukopenia, Anemia, vasculitis, subcutaneous edema, hepatic necrosis
Cockatiel appear to have inherited resistance to infection

Question 13

Female 2 a, GP; chronic history of lethargy weight loss and regurgitation; what do you see on the radiograph
1 how can proventricular size be evaluated radiographically in psittacines?

2 What diseases could result in similar radiographic findings?

Answer 13

Radiograph: moderate dilation of proventriculus and ventriculus + severely gas distended, hour glass shape I asymmetrical and dilated on the left sife, proventriculus extend laterally beyond liver margin+
Using proventriculus:keel height ratio; in lateral projection: Proventricular diameter measured at the level of junction between thoracic vertebrae and synsacrum and perpendicular to the long axis of proventriculus; keil height : measured as the maximum dorsoventral height ; ratios <0.48 indicate that the proventricular diameter is normal ; ratios >0.52 are consistent with proventricular diseases
PDD, nonspecific proventriculitis; heavy metal toxicosis, foreign body, koilin dysplasia, neoplasia, M.O., helminth infection

Question 14

Name 4 drugs used to treat PDD and ode of action:
2 groups of drugs supportive therapy:
Is PDD a lethal diseases?

Answer 14

NSAIDS Celecoxib COX 2 inhibitor
Tepoxalin NSAID combined COX 1 COX 2 and 5 lipoxygenase inhibitor
Cyclosporine T cell inhibitor
Amantadine Hydrochloride: antiviral

GI motility modifiers
AB and Antifungals – sec infections

Not necessarily, esp when treatment is initiated at early stages of diseases

Question 15

158: Crop biopsy of cockatoo with lymphoplasmacellular infiltration of myenteric ganglion:
Characteristic for?
Key points for preparation + collection of crop biopsy:

Answer 15

PDD

Suff size (12x8mm)
Include prominent blood vessel along long axis- increases the probability to onclude suff nervous tissue
Small tissue sample kept without fixation for RT PCR

Question 16

188 Lymphoplasmacytic perivascular cuffing in the brain of a blue and gold macaw with PDD
Characteristic for?
Lesions always associated with CNS signs in psittacines?
Other histological lesions suspected?

Answer 16

In birds with PDD, but alo WNV, PMV f.i

No! Commonly seen without CNS signs in birds with PDD

Lymphoplasmacytic mesenteric ganglioneuritis; lymphoplasmacytic infilitration of medullary areas within the adrenal gland; lymphoplasmacytic myositis in the ventriculus, lymphoplasmacytic infiltration of epicedial ganglia, lymphplasmatic cardiomyositis, lymphoplasmacytic cuffing of peripheral nerves, perivascular cuffing of optic nerve- choroids, ciliary body and occasionally iris and pectin, retinal lymphoplasmacytic infiltration and retinal degeneration

Question 17

How many psittacid Herpesvirus are currently known?
Which one is capable of inducing Pacheco?
Which one is capable of inducing mucosal Papillomas?
Which one is capable of inducing Resp.Diseases?

What is the nature of Herpesvirus ?

Answer 17

1-3
1 Pacheco
1 und 2(GP) mucosal Papilloma
3 Resp Diseases

Enveloped DNA

Question 18

How many psittacine Herpesvirus-1 , genotypes?
Which genotype is most likely to induce mucosal papillomas and Bile duct carcinomas?

What is the appr. Incubation period?

Which species are susceptible?

Answer 18

4 Genotypes
Genotype 3, esp in Amazons

Incubation about 5-7 days

All species susceptible – mucosal papillomas esp new world parrots amazons, conures, macaws , hawk head parrots

Question 19

What clinical signs can be expected with Pacheco Diseases?

Post mortem lesions?

Answer 19

Unexpected/ multiple deaths in a collection, unspecific signs- some biliverdin stained urates (yellow/green) prior to death

Pm most birds excellent BodyCondition; gross lesions: subtle changes diffuse lipidosis to marked spleno and hepatomegaly with multifocal areas of discoloration ( necrosis), some gross evidence of pancreatitis + enteritis (certain genotypes), intralesional inclusion bodies: Pan-nuclear eosinophilic

Question 20

Psittacine Herpesvirus 1 pos.. flock:
Diagnosis?
Treatment?

Vaccination?

Answer 20

PCR oral + cloacal swab (blood less sens.); serology (all 3 genotypes!)

Acyclovir seems high effective to prevent mortality but birds stay carriers!

Developed, may useful in high risk flocks, still unkown if vaccine from one serotype protects against others

Question 21

Psittacine Herpesvirus-2:
Which species is most likely to be affected?

What would be the DD?

Diagnosis?

Answer 21

GP;
DD: parrot Papillomavirus 1 ( rarely and only wild caught birds so far) neoplasia

Characteristic lesion, biopsy: fibropapillomatous lesion without virus inclusion bodies
PCR oral and cloacal swab

Question 22

Psittacid Herpesvirus-3:
In which species described outbreaks?

Clinical Signs?

Pm findings?

Answer 22

Eclectus and Bourkes parrots

Resp: coughing , diff breathing, nasal discharge, death within 3-7 days

Conjunctivitis, tracheaitis, pneumonia/ airacculities; syncyitical cells + pannuclear eosinophilic inclusion bodies in bronchi + paranbronchi

Question 23

Gallid Herpesvirus 2: Which forms possible + typical signs

Pathohistological findings? – most likely DD ?

Typical age? Mortality rate?

Answer 23

Classic marek/ neurolymphomatosis: asymmetric paralyses (1 leg/ wing, + pale visceral tumors)
Acute Marek: explosive outbreaks- depression in a large proportion of the flock , after few days ataxia, paralysis
Occular lymphomatosis: iris gray in color- partial/total blindness; lymphoblastoid cell infiltration
Cutaneous Marek: round nodular lesions upt to 1 cm in diameter; esp at feather follicles
Transiet paralysis: (by vasogenic cerebral edema) for 24-48 hours- birds can recover
Chronic Marek: Immunsuppresion

Mononuclear infiltration within peripheral nerve, other tissue / organs
Gross: nerves thickened ( up to 3 times) discolored with loss of cross striation #
Lymphomatous lesions (like in avian leukosis) in gonads, heart , proventr, , lungs, seldom Bursa of Fabricius (most commonly affected by leukosis!)

2-5 months; up to 80%

Question 24

Gallid Herpevirus 1:
Common clinical signs?
Common Age?
Mortality Rate?

PM findings?

Answer 24

ILT
High contagious resp diseases, distressed breathing, loud gasping, + coughing, expectoration of mucus and blood
Mild to peracute, mortality 2-50% ; reduced egg production
Common 4- 18 months

Necrosis, hemrorrhages, ulcerations, formation of diphteroid membranes; bloody mucoid pseudomembranes at the trachea ( dead due to asphyxia)

Question 25

Duck Plague: Common Signs? Morbidity/ Mortality? Pm Lesions?

Answer 25

Depression, drop in egg production, ruffled/dull feathers, ocular nasal dicharge, labored breathing; anorexia; watery diarrhea; thirst ataxia and death Morbidity and mortality 5- 100 % PM: vascular damage, hemorrhage, GI tract +body cavities ; petechial hemorrhage and focal necrosis

Question 26

135: sudden death of 24 from 60 death waterfowl within 24 hours in spring, cloaca surrounded by blood: Most likely etiology? Pm findings? How to manage outbreak ? Prevent future outbreaks?

Answer 26

Duck plague/ duck viral enteritis; seasonal diseases: anatid Herpesvirus 1 Vascular system attacked: hemorrhage in esophagus, GI tract ; generalized hemorrhage Birds usually not found alive Depopulation cleaning and disinfection , repopulation with vaccinated stock : mortality up to 90-95 % surviving birds lifelong carriers with seasonal sheddings- creating high risk to any unvaccinated bird Annual vaccination 2 months before risk periods; only life attenuated vaccines are effacious

Question 27

Raptor Herpesvirus: Which herpesvirus are known? 2 are identical to pigeon Herpesvirus 1- which ones? Which species most affected? Clinic PM Most likely source of diseases?

Answer 27

Falconid, strigid and accipitrid Herpesvirus Falconid and strigid Gyrfalcons + Hybrids Fatal diseases: sudden death- depression , weaknes, anorexia, regurgitation –> death ; lime green urates; Survivors: lifeling infection and intermittend shedding possible! PM: multifocal necrosis aof liver and spleen pigeons

Question 28

Pigeon Herpesvirus: Other name of diseases Typical age of diseases? Clinic? PM? DD?

Answer 28

Smadel Diseases 1 – 6 months Difficult breathing, regurgitation, stop feeding, difficult in feeding, green- watery feces; mortality 24-48h up to 15 % Damage of the upper digestive tract coated with white- yellow necrotic debris: DD severe trichomoniasis, candidiasis, diptheroid pox

Question 29

PBFD: How many genotypes known? Transmission? Incubation Period? Tenacity? Nature?

Answer 29

Over 200 genotypes known Incubation 21-25 days up to months /years Oral /intracloacal ingestion? Vertical ? Tenacity in Environment high, in contaminated nests , up to years infectious! Nonenveloped DNA

Question 30

5 month old GP; lethargy, decrease of vocalization inappetence, clinical exam: mildly dehydrated; bright yellow urates; hematlogy: moderate anemia, nonregenerative; severe leukopenia- with absence of heterophils Most likely diagnosis? Additional Tests? Treatment, prognosis?

Answer 30

Circovirus Serology (HA+HI); PCR feathers (high risk of contamination), blood TH: mainly supportive, IFN alpha described in other Circovirus, Cytokine, chicken interferon gamma, D D-glucan from oyster mushroom GP high susceptile (as well as black cockatoos) often die before clinical signs

Question 31

PBFD: Acute diseases most likely in which species? Clinic? Hematological and Biochemistral pathologies?

Answer 31

GP nestling and fledgling: depression, green diarhhea; anorexia regurgitation ; pterylodynia (feather tract lesions): edematous painful wingtips hema: leukopenia (heteropenia lyphopenia); anemia; reduced TP; reduced prealbumin and red Gammaglobuline

Question 32

72 24 month old cockatoo; tatty plumage, slightly skinny; bright shinig beak 1 immediate concern? 2 how to confirm diagnosis? Action to clear infection from the collection? 3 how to eliminate pathogen from the environment and prevent spreading

Answer 32

Abnormal shiny beak, typicall associated with circovirus (nonenveloped DNA) . to the loss of powder down feathers Confirmation by OCR of feather pulp( blood) (Feather plumes avoided- false pos due to contamination possible) Serology; Biopsy of skin /developing feathers )low sensitivity); Histo: basoph intracytoplasmatic inclusions in macrophages f feather pulp, in epithelial keratinocytes-also intranuclear inclusions); and basophilic inclusions in Kupfer cells of liver; IHC esp of Bursa of Fabricius, feather follicle, spleen , esephagus + crop Birds tested pos. without clinical signs: Retest after 30 days- clearance is possible; all contact birds tested; test and removal policy in breeding collection adviced   Infection spread by feather dust ; disinfection by fogging with disinfectant of proven activity (Virkon S) ; if uncontrolled can stay infectious about 2 years! Regularly weekly fogging with suitable disinfectant and record keeping of clinical areas recommended  

Question 33

PBFDV Histopathological Findings IHC which organs? Diagnosis Therapeutics

Answer 33

Basophilic intracytoplasmatic IB in th macrophages of feather pulp and epothelial keratinocytes and in Kupfercells (liver) ICH: Bursa of Fabricius, Feather follicles; spleen, esephagus, crop Clinic, Biopsy of Skin and Developing feathers (low sensitivity) Serology ( HA HI) PCR feathers ( high contamination risk) Blood Tx: Interferon alpha; Cytokine, Interferon Gamma ; D glucane from oyster mushroom

Question 34

90: Budgie with signs of PBFD- 1. which lab test offers highest correlation with the diseases? 2. How many different genotypes of PBFD exist? 3. Would genetic variation interfere with diagnostic testing?

Answer 34

1. Presence of high virus ag titers shed from feathers- measurable by hemagglutination activity (HA), diagnosis of PBFD clinic/ histopathological lesions . fether dystrophy , feather loss; basophilic intranuclear inclusions; ; PCR tests also detect viral DNA in clinical normal birds, andbirds that are recovering from infection- best sample blood: less risk of contamination using feathers 2. Over 200 diff genotypes 3. Ideally 2 methods of detection should be used to validate test results- PCR and antigen detection ; or 2 PCR assays targeting 2 regions of the virus genome

Question 35

Pigeon Circovirus: Age + Clinic? Transmission?

Answer 35

4 weeks- 4 months ; lethargic, anorexia, green watery feces; sometimes crop stasis: some deteriorate and die, many recover within a week Part of young pigeon diseases ( + sec infections) ` Horizontal + vertical

Question 36

Polyoma: Nature? Pathogenesis- major factor ? Common affected species? clinic Difference to PBFD?

Answer 36

Papoavirida: nonenveloped DNA Age of the bird at time of infection- presistent infected birds may those who where infected before they are immunocompetent Budgies and Neophema Sudden death of neonates, without signs, hatchlings 30-100 % mortality rate; abdominal distension, SC hemorrhages, tremors-head + neck, ataxia ; decr formation of down/ contour feathers Survivors; sym feather abnormalities- dystrophic primary and tail feathers; lack of down feathers on abdomen and back; lack of filoplumes on head and neck; Symptoms resolve after few months_ unlike in PBFD!

Question 37

Polyoma other Psittaciformes: Clinic acute diseases Chronic form In Adults? Which species seems to be more resistant to develop diseases? Other species than psittaciformes with acute mortality after infection?

Answer 37

Acute: peracute death, ,depression, anorexia, weight loss; delayed crop passage ,regurgitation; diarrhea dehydration; sc hemorrhages, dyspnoe, PU ; CNS digns possible; fledglings usually die 12 to 48 hours after clin symptoms Recoveríng birds: asympt. Carrieres! chronic.: weight loss, anorexia, PU, recurrent sec. Infections; poor feather formation; recovering birds appear normal, ie because of acute glomerulopathy/renal faulure Adults: only occassional clinical signs, subclinical carriers Cockatoos finches

Question 38

Polyoma: Pathology Diagnosis

Answer 38

Large clear basophilic or amphophilic intranuclear inclusion bodies in heart/liver/spleen/ GI tract/ skin/pancreas/brain-….) Immune complex induced glomerulopathy; esp larger psittacines: massive hepatocellular necrosis Highest virus con in brain ! IHC, Serolog (not routinely available), PCR blood and cloacal swab

Question 39

Polyoma: Outbreak in a collection- Advice to the owner? Vaccination? Disinfection?

Answer 39

Eradicate horizontal transmission between birdsa nd between clutches of young birds- identify carriers and isolate them; accurate record keeping and diseases monitoring; complete cessation of breeding activity for 6 months may eradicat infection+ hygiene and disinfection Vaccine in some countries available; controversial effectiveness; likely to ptotect fledglings from APV free aviaries- valuable tool togethet with hygiene measurements Chlorine, synthetic phenol, chlorine dioxide, sodium hypochlorite, 70 % ethanol, air filtration systems

Question 40

196- Passeriformes severe losses of nestlings 4 days- 6 weeks;diarrhea, death within 24-48 hours, adult birds not affected, no drop in egg production / hatchability. Virus particle on electron microscopy: What virus most likely cause of problems in these nestlings? Findings expect on histopathology? How to confirm diagnosis? Necessary steps to clear virus from collection ?

Answer 40

Avian Polyomavirus Large basophilic intranuclear inclusion bodies in many organs, often membranous glomerulopathy; Diagnosis confirmed PCR techniques Stop breeding for a complete season to minimize virus shedding; test all breeding birds with choanal and cloacal swabs; be aware of intermitted shedding; eliminate shedding birds:: test and quarantine new admitted birds: closed aviary ( no visitors) use foot disinfection, disinfect hand, tools, food and water balls and tools

Question 41

HPAIV: Post mortem lesions Nature of AIV

Answer 41

Peracute death- no gross abnormailities Sc edema head and upper neck and feet Cyanosis + hemorrhage wattles + combs Hemorrhage viisceral organs- esp epicard, pectoral muscle, mucose of ventr and proventr. Necrotic foci pancreas, spleen and heart Enveloped RNA

Question 42

AIV: Preventative measurements Vaccination?

Answer 42

Monitor movement of poultry between farms and markets Monitor birds in live markets- exports and imports Improve Biosecurity measurements (shilded enclosures to prevent droppings from wild birds, prevent contact with wild birds (esp aquatic birds) Separate land based pultry, pigs, aquatic birds on farms and markets In case of acute outbreak- close live poultry markets, keep poultry indoor Seroloical and other epidemiological studies in wils birds- to determine wheter HPAIV ist established in wild birds Vaccination- restricted my government Prevents against diseases and mortality does not neccessarily prevent infection!; but higher does of infectious virus is required and vaccinated birds shed less virus Neg: delayed diagnosis of infection spread of virus Only in special situations allowed (zoo outbreaks, valuable animals) only useful in combination with improved Biosecurity:hygienic measurementsm selective culling, isolation, antiviral treatment, disinfection of the area; monitoring fo vaccine efficianc and shedding of field strains

Question 43

AIV: Useful disinfectants

Answer 43

Easy to inactivate because of outer lipid layer with detergents and sopa; Oxidizing agents Alkalis Acids (citric acid) Formaldehyd gas Temp Activated at 56°C for 3 hours; 60°C 30 minutes, conventional cooking (core temp.70°C ) sufficient to iinactivate cooked poultry safe food

Question 44

AIV: Therapy?

Answer 44

Neuraminidase inhibitors (Oseltamivir, Zanamivir); ion channel of M2 membrane protein inhbitor (Amantadine, Rimentadine) Rapid resistency of AIV against these drugs during treatment!

Question 45

Usutu: Nature? Common species affected? Most important Vector in Europe? Subtypes of these vectors? Seasonal peaks in EU?

Answer 45

Enveloped RNA Blackbird, great grey owls, in general clinical diseases Passeriformes and Strigiformes Culex pipiens – pipiens seasonal active mainly ornithophile, most common - molestus, autogenous, active through hole year , mammophilic esp. Atrhrophilic US many hybrids! Opportnistic feeders- major contributor to outbreaks of WNV in US Peaks July to mid Sept

Question 46

Usutu: Diagnostics- Viremia? which serological tests available? Which for screening ? Which is gold standard?

Answer 46

Only short viremia 2 days Followed by serological response: IgM, + seroconcersion to IgG; or 4 tim rise in titer taken 10 days apart; false pos results possible Serlogical screening – HI Haemagglutinin Inhibitation test- cross reaction with other Flavivirus! More specific/ gols standard PRNT plaque reduction neutralization test (cross reactions also occur!) Most reliable Usutu specific PCR (RT) brain tissue

Question 47

Flavivirus: Measurements to prevent mosquitos?

Answer 47

Prevent stagnat pools of water Keep animals that reduce the lava in the pools/ holding tanks (fish, terrapin, crustaceans..) Indoor housing of immunologic naive species during high season ( in case of usutu strigiformes and passeriformes) Mosquito screens on windows and doors Air conditioning during critical months Regular treatment agains ectoparasites

Question 48

WNV: Laboratory Criteria to diagnose WNV Serological Tests- For screening? Which one is more specific? AB persitency? At what time PI infectious WNV can be detected in sera/ swabs Tissues?

Answer 48

At least 4x rise in virus specific serum titer , paired sera 2-4 weeks apart Virus isolation (gold standard); viral specific antigen +ICH, genomic sequecing (RT-PCR): tissue (Kidneys, spleen, brain, heart/ antemortem oropharyngeal /cloacal swab/ feathers)/ bloos, CSF (cerborspinalfluid)/ other bidy fluids Virus specific IGM AB in CSF by ELISA Or in serum- confirmed by virus specific IGG AB in the same/ later speciimen by another serological assay ( neutralization or hemagglutinin inhibitation) AB Cross reaction with other Flaviviruses!! Serological Tests: Hemagglutinin Inhibtation ; „blocking ELISA“ developed for broad species used; - confirmation by PRNT (more specific) needed- cann differentiate between St Louis encephalitis and WNV Variable AB persistency in naturally infected birds, fi in rock pigeons AB over 15 months! 1-7-10 d PI in sera/Swabs 2-3 weeks in tissues

Question 49

WNV: Which species competent reservoir? Which species highly susceptible?

Answer 49

Reservoir: Passeriformes (blue jay, common grackle, house finch, American crow, house sparrow) and Charadriiformes Susceptible: Corvidae, Raptors esp Strigidae

Question 50

WNV: Viremia? Shedding of the virus how many days PI Serological titers? How long detection in tissues? Antibody detection?

Answer 50

Viremia day 1-7 Shedding 1-3d PI intermittend till day 14 or more Titers day 2-4 PI Detection in tissue up to 27 days PI AB from 5-7 days PI, raise 4times/more within first months; AB persit and protect againt infections for 4 years or longer

Question 51

WNV: Preventive Measurements

Answer 51

Reduce contact between anímals/Humans and mosquitos: Chemical – inseciticides Biological. Mosquito eating predators; Mechanical, mosquito nets/screens/ drainage and irrigating systems, eliminate standing water, fill holes, covering containers Vaccination: killed and recombinant virus available; lack of evident data for birds, reduced seroconversion, depends on the species and vaccine construction + application

Question 52

106 Cockatoo suspected WNV: Diagnostic tests ante mortem: Prognosis: Gross post mortem: treatment:

Answer 52

Oropharyngeal and cloacal swabs- PCR ; PCR blood. Could be false neg. because of rapid clearance of WNV from bloos; peak viremia about 2-4 days pi; paried serological samples; Plaque neutralization test – gold standard for WNV antibody detection but cross reactivity is possible  other AB tests—blocking ELISA- used for high throughput screeining ; virus isolation gild standard for confirmation of WNV infection Guarded to poor No significant lesions- mild moderate enlargement of lover and spleen Histopatho: lymphoplasmacytic and histiocytic hepatitis, interstitial nephritis; myocarditis splenitis, enteritis, pancreatitis, encephalitis might be seen pM diagnosis: virus isolation/ RT PCR testing of homogenized tissue ( kidney, spleen, heart and brain; detection in tissue 2-3 weeks PI supportive care ; sec infections

Question 53

Newcastle: Nature? Known serotypes birds? Which most important? Tenacity ? Disinfectants?

Answer 53

Enveloped RNA PMV1; most important 2 +3 – in Passeriformes and Parakeets, resp and enteric doseases, CNS signs, similar to PMV 1; PMV 2also in chickens and turkeys, PMV 3 turkeys PMV 6 in ducks and geese /asymptomatic) rarely resp signs in turkeys PMV 7 high prevalence in pigeons and ducks; occ mild resp signs turkeys Heat stable, remains infectious in bone marrows and muscles of slaughtered chickens at -20°C at least 6 months! At 1 °C 134 days! In dried mutes several years Quaterny Ammonium compounds, Lysol, Cresol, Formalin

Question 54

225Which PMV serotype most likely? Other possible serotypes?

Answer 54

PPMV 1; APMV 2 chickens and turkeys, APMV 3 turkey and parakeet; APMV 4 wild and mallard duck; goose and chicken; APMV 5 budgerigar; APMV 6 doemstic and mallard duck, goose, turkey, APMV 7 wild dove, turkey sotrich, APMV 8 wild Canada goose, pintail, APMV 9 domestic and feral duck; APMV 10 rockhopper penguion , APMV 11 common snipe; APMV 12 wigeon

Question 55

PMV: Virulence stages and index?

Answer 55

Virulence measured with neuropathic index by intracerebral incoluation of day old chicks NI 0.25 lentogen NI 0.6-1.9 mesogen NI2.9 velogen

Question 56

PMV1:Pathotypes and clinic

Answer 56

5 pathotypes: 1. Viscerotropic velogenic: high mortality, swelling of tissue around the eyes; bloody diarrhea, hemorrhaic lesions in proventriculus and intestines 2. Neurotropic velogenic: high mortality; resp and CNS signs; paresis of limbs, wings, ataxia, torticollis, circling, tremor 3. Mesogenic: resp signs, occasionally CNS signs- head tics (es falcons); low- moderate mortality 4. Resp. Lentogenic mild- subclinical resp. 5. asymptomatic enteric subclinical enteric  No clear cut! Overlapping in all species !!!!!!!!

Question 57

PPMV: Clinical signs Chickens Pigeons , quails, houbara bustard Falcons Vultures Hawks and buzzards Hawks and eagles

Answer 57

Chickens: depression, drop of egg production/ cessation, diarrhea, CNS signs paralysis torticollis Pigeons, quails houbara bustards: diarrhea CNS signs , PU? Falcons: Gi signs (anorexia, vomiting, paralytic ileus); later also CNS signs (ataxia, head tics, tremors, paresis of wing and legs,(rarely torticollis- samour vs BSAVA classical torticollis ); usually fatal within 48 h Vultures: appear resistant to infection Hawks and buzzards- anorexia may be the only signs Hawks and eagles: nonspecific signs, varyying intensity; CNS-resp-renal-GI

Question 58

PMV: PM Gross lesions Diagnosis

Answer 58

No pathognomic groos/ microscopic lesions Hemorrhagic lesions in intestine, petechial bleeding proventriculus; hemorrhagic changes resp tract Virus isolation; to exclude viruses of low pathogenicity which are ubiquitous in feral birds and to exclude live vaccines Of slpeen ´, brain, lung Allantoic inoculation of 10-12 day old embryonated eggs/ tissue culture chicken embryo fibroblasts Assesment of viruelnce: intreacerebral or intravenous pathogenicity index mean death tie by inoculation in the allantoic cavity of 9-10 days old embryos: under 60 h to kill lentogen 60-90 h to kill mesogen over 90 h to kill velogen RT PCR

Question 59

PPMV: Infected pigeons lifelong carriers? Incubation period clinic

Answer 59

No- stop excreting the virus 6-8 weeks after infection Incubation Period : 5 days- 6 weeks Clinic: interstitial nephritis: PU, PD; watery green feces; CNS: loss of balance, inability to pick feed; torticolis, unilateral/bilateral paralysis, loss if rightning reflex; circling, somersaulting, flying backwards, tremor of head and neck Low mortality in adults, can be hight in young pigeins Recovery possible from mild CNS signs and diarrhea, from severe CNS signs some birds might recover

Question 60

PPMV-vaccine?

Answer 60

Inactivated vaccines, sc, from 3-4 weeks of age, adults 3-6 weeks before onset of breednig/ racing season

Question 61

Poxvirus: Nature? Forms?

Answer 61

Enveloped DNA Cutaneous forms-scabs of unfethered skin; major vector anthropods; also direct contact with infectious material + abrasions/cuts Diphteric form: mucous membranes with pale/yellow lesions, turns into septic7 systemic form;

Question 62

Poxvirus, Patho:

Answer 62

Erythematous macula. Papular-> vesicular-> pustula-> ruptures-> crust formation Histo: cytoplasmatic swelling, vacuolation, balloning degeneration , inclusion bodies „Bollinger Bodies“ or elementary Bodies (Borrel bodies)- spec staining methods Wetpox: discrete pale/ yellow lesions , raised necrotic lesions of oropharyngeal mucosa, mucoid tracheitis, rhinitis

Question 63

Poxvirus; Treatment? Prevention?

Answer 63

Treat/prevent sec infection Clean lesions with polyvidone iodine Vit A supplementation Avoid stress, good husbandry Most pox: speciesspecific Live attenuated vaccines available varyying degree of success; insecticide spraying

Question 64

Saker falcon and raven presented with digital lesions. Demonstrated Diseases? Ethiology? Treatment and Preventive Actions

Answer 64

Dry and wet form pof Poxvirus Avian Poxvirus (Avipoxvirus spp.) Enveloped DNA Virus, causes diseases in over 200 species of birds, currently 10 diff species of poxvirus known for each of whom diff bird species are the natural hosts Transmitted by ingestion of contaminated food and water, aerosols, biting insects, arthropods, 2 forms cutaneous form- wart like growths around eyesand other feather free areas (apterylae) Diphteric/ wet form- raised yellow blemishe on the mucous membranes of the mouth esephagus trachea, lungs, areas of transparency on the skin which change to brown scabs as the mature Preventive actions: prevent standing water , decontaminate feeders/ perches cages Vaccines: devolped for strains of poxvirus (fowl, canary, pigen, quail) as they tend to be taxon specific –varyying success in / for other species Treatment- Sec infections: Antibiotics, local. Iodine application, Vit A supplementation

Question 65

Pigeon Adenovirus: Classic clinical presentation ? What age? Transmission?

Answer 65

Birds > 1 year; inclusion body hepatitis- damage to intestine and crop, intestinal stasis, sec infection with esp E coli and yeasts; typical outbreaks few days after racing Green feces, PD; vmiting, crop stasis Most birds reciver within 4-6 days; but sme die within 24 hours esp because of sec infections Horizontal- fecal oral (vertical important in poultry!)

Question 66

IB, Coronavirus: Nature Clinic? Incubation period? Age? Mortaility?

Answer 66

Enveloped RNA 24-48 hours incubation All ages, more sever/ fatal young birds Clinic: Resp. Signs, gasping, sneezing, tracheal rales; nasal discharge, wet eyes, swollen sinus After resp phase nephropathogenic strains can cause PUD/PD, impaired growth and mortaility Layers: reduction in egg production (sudden ónset up to 3 weeks) ; eggs thin rough and misshappen shell, typical longitudinal + transversal rills Mortality can reach 25 %

Question 67

Answer 67

1. marble spleen diseases: ring necked pheasants, 3-8months old birds 2. Smadel: Pigeon Herpesvirus 1, pigeons (owls+raptors) 3. Fowlpox: enveloped DNA 4. Usutu: Flavivirus 6.Duck Plague/Duck Viral Enteritis; enveloped DNA 7. Bornavirus: enveloped RNA; Psittaciformes, various avian species 8 Herpes?

Question 68

248: Young red bellied parrot died acutely- pm splenomegaly hepatomegaly; impression smear: karyomegaly – what etiologic agents considered? Diagnostic tests to confirm diagnosis?

Answer 68

2 most likely causes of karyomegaly Avian polyoma and adenovirus PCR + histopathology. Basophilic intranuclear inclusion and karyomegaly and necrosis in liver in spleen- possible In acute Polyoma and adenovirus infections

Question 69

114: farm: sudden death of majority of ducklings- CNS signs/ acute death: Top DD Pathological changes necropsy: Tests:

Answer 69

Duck hepatitis virus (Picornavirus- nonenveloped RNA); hepatomegaly with hemorrhagic foci, splenomegaly, swelling of the kidneys, congestion of renal vasculature Virus isolation from liver tissue; virus neutralization + PCR also available

Question 70

62 Vaccines in pigeons for 4 different infectious agents: What is known about the preventive efficacy of each of these vaccines? Which routes are used? Recommended protocols for each?  

Answer 70

APMV (considered fully protective) Pigeon Pox (considered fully protective) Pigeon Herpesvirus (no scientific reports available) Salmonella typhimurium var. Copenhagen (partial protective)   Route subcutaneously in the neck, one form of Poxvaccciine topically into feather follicles of pluckes feathers   Protocols: Pmv from 3 weeks on; from 5 weeks on Salmonella, Pox, Herpes Booster 2-4 weeks later for Herpes and Salmonella Yearly revaccination recommended. At least 3 weeks prior to their first flight in racing season

Question 71

List several characteristic why birds are predisposed to respiratory aspergillosis

Answer 71

High Body Temp Absence of Epiglottis absence of diaphragm and lack of powerful cough limited ciliated epithelium greater respiratory surface area and thinner air blood capillary barrier poorly vascularized air sac system(warm and oxygenated air sac system favorable conditions for vegetative growth and sporulation of Aspergillosis) unidirectional air flow in lungs + directional airflow in air sacs, hinder elimination of inhaled particles

Question 72

Why antibody response are unreliable diagnostic tool for aspergillosis ?

Answer 72

AB production trail behind Antigen exposure by 10-14d, low AB Production in Immunosuppressed results in false negative, high AB titers can be found in healthy birds, in general low specificity and sensitivity

Question 73

How to disinfect a cage with a chlamydia

Answer 73

Low concentration of Formaledhyde, Benzalkonium chloride, Hydrogen Peroxide (also inactivated with UV, 70% ethanol) (quaternary Ammonium salts and lipid solvents not a good choice)

Question 74

Chlamydia elementary bodies- stains

Answer 74

Giemsa (elementary body + reticulate body blue), Macchiavello, Gimenez, Stamp, Castaneda stain